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目的:研究细胞凋亡在新生儿缺氧缺血性脑损伤(HIBD)中的作用.方法:结扎新生7D龄大鼠左颈总动脉后吸8％浓度氧2H制成HIBD模型,应用苏木素－伊红(HE)染色、原位缺口末端标记(TUNEL)、DNA电泳分析综合研究新生大鼠HIBD后脑细胞的死亡形式.结果:缺氧缺血(HI)后0HHE染色即发现左侧纹状体有一些神经元呈凋亡早期的改变;HI后18HTUNEL染色在左脑皮质及纹状体见到阳性凋亡细胞;HI后2DDNA电泳见到DNA梯形带;HI后2~3D凋亡达高峰;持续至少21D.结论:3种方法均表明细胞凋亡为HIBD后神经元的主要死亡形式,也是加重脑损伤的一个因素.“,”Objective: The objective was to assess the potential contribution of apoptosis to neuronal death after hypoxic ischemic brain damage (HIBD) in the neonatal rat. Methods: The unilateral carotid artery of 7 day old. Wistar rats was ligated and the rats were kept in an hypoxic (8% oxygen) enviroment for 2 hours to produce the HIBD model. The patterns of neuronal cell death after cerebral hypoxic ischemic (HI) injuries were examined in neonatal rat using Hematoxylin and Eosin (H and E) staining, terminal deoxynucleotidyl transferase mediated dUTP biotin nick end labelling (TUNEL) staining and electrophoresis analysis. Results: The results showed that some neurons in striatum revealed early morphological characteristics of apoptosis by H and E staining at 0 h after (HI); The positive apoptotic cell was not detected in cortex, striatum of the ipsilateral hemisphere until 18 h after HI by TUNEL staining; Laddered DNA was found at 2 day after HI by DNA gel electrophoresis; Apoptosis peaked at 2~3 day after HI; and persisted for 3 weeks. Conclusion: Three methods suggested that apoptosis was a major form of cell death after cerebral HI in the neonatal rat, and was also a factor that exacerbated infarct area after HI.